The treatment of psychiatric disorders by surgical means has an extensive history. In the early 1930's, Fulton and Jacobsen first recognized that experimentally induced neurotic behavior in chimpanzees could be abolished by frontal lobectomy. Within a few years, Freeman and Watts developed the first psychosurgical procedure for humans known as the frontal lobotomy.
As the inherent physiology of the frontal lobe became more evident, the original freehand procedure of Freeman and Watts became less and less extensive. By the late 1940's, the method of stereotaxis, in which the patient's brain is modeled in 3-dimensional space for exquisite targeting accuracy, merged with lesioning techniques resulting in an even more efficacious and safe psychosurgical procedure. Further developments of stereotactic equipment have combined with novel advancements in functional and anatomic imaging as well as intraoperative electrophysiological mapping to encompass the state of the art in the neurosurgical treatment of neurological and psychiatric disorders today.
While technologically improved and more precise, lesioning techniques have the fundamental limitation of being inherently irreversible and are essentially a “one shot” procedure with little chance of alleviating or preventing potential side effects. In addition, there is a limited possibility to provide continuous benefits as the disease progresses and the patient's symptoms evolve.
Within the field of neurosurgery, the use of electrical stimulation for treating neurological disease, including such disorders as movement disorders including Parkinson's
Within the field of neurosurgery, the use of electrical stimulation for treating neurological disease, including such disorders as movement disorders including Parkinson's disease, essential tremor, dystonia, and chronic pain, has been widely discussed in the literature. It has been recognized that electrical stimulation holds significant advantages over lesioning since lesioning destroys the nervous system tissue. In many instances, the preferred effect is to modulate neuronal activity. Electrical stimulation permits such modulation of the target neural structures and, equally importantly, does not require the destruction of nervous tissue. In many ways, this is analogous to a reversible and adjustable lesioning procedure.
To date, however, disorders manifesting gross physical dysfunction, not otherwise determinable as having psychiatric and/or behavioral origins, comprise the vast majority of those pathologies treated by deep brain stimulation. A noteworthy example of treatment of a gross physical disorder by electrical stimulation is included in the work of Alim Benabid, who developed a method of reducing the tremor associated with Parkinson's disease by the application of a high frequency electrical pulse directly to the thalamus. This has also been applied in the subthalamic nucleus for the treatment of Parkinson's rigidity, slowness of movement, walking and other movement (see e.g. the New England Journal of Medicine, Vol. 339, October 1998, pp. 105-1111, Electrical Stimulation of the Subthalamic Nucleus in Advanced Parkinson's Disease).
Efforts have been made to treat psychiatric disorders with peripheral/cranial nerve stimulation. A recent investigational protocol has demonstrated partial benefits with vagus nerve stimulation in patients with depression (Biological Psychiatry 47: 216-286, 2000) Additional clinical trials with depression and vagus nerve stimulation are underway. Another noteworthy example is the effort to control depression and compulsive eating disorders by stimulation of the vagus nerve is provided in U.S. Pat. No. 5,263,480. This treatment seeks to induce a satiety effect by stimulating the afferent vagal fibers of the stomach. For patients having weak emotional and/or psychological components to their eating disorders, this treatment can be effective insofar as it eliminates the additional (quasi-normal) physio-chemical stimulus to continue eating. This is especially true for patients who exhibit subnormal independent functioning of these fibers of the vagus nerve. For compulsive eating patients who are not suffering from an insufficient level of afferent vagal nerve activity resulting from sufficient food intake, however, the over stimulation of the vagus nerve and potential resultant over abundance of satiety mediating chemicals (cholecystokinin and pancreatic glucagon) may have little effect. It has even been suggested that continued compulsive eating, despite overstimulation of the vagus nerve, may exacerbate the emotional component of the patient's disorder. This, therefore, begs the question, of whether vagus nerve stimulation is useful in treating the psychological component of the disorder of compulsive eating, or is it simply a method of minimizing the additional, but natural, pressures to eat because of normal physical hunger. More generally, the question may be asked, is peripheral nerve stimulation of any kind the most appropriate method of treatment for disorders that are, at the core, the result of a pathology exhibited in the brain. The effect of this peripheral stimulation seems to be non-specific and a secondary phenomenon. Indeed functional brain imaging studies have demonstrated induction of intracranial thalamic activity thus providing evidence for an indirect action of the peripheral stimulators. A more appropriate target may be the brain region which is functioning abnormally.